Inverse correlation between gastroesophageal reflux disease and atrophic gastritis assessed by endoscopy and serology

BACKGROUND Helicobacter pylori(H.pylori)infection is known to prevent the occurrence of gastroesophageal reflux disease(GERD)by inducing gastric mucosal atrophy.However,little is known about the relationship between atrophic gastritis(AG)and GERD.AIM To confirm the inverse correlation between AG and the occurrence and severity of GERD.METHODS Individuals receiving health checkups who underwent upper gastrointestinal endoscopy at Seoul National University Healthcare System Gangnam Center were included.The grade of reflux esophagitis was evaluated according to the Los Angeles classification.Endoscopic AG(EAG)was categorized into six grades.Serologic AG(SAG)was defined as pepsinogen I≤70 ng/m L and pepsinogen I/II ratio≤3.0.The association between the extent of EAG and SAG and the occurrence and severity of GERD was evaluated using multivariate logistic regression analysis.RESULTS In total,4684 individuals with GERD were compared with 21901 healthy controls.In multivariate logistic regression analysis,advanced age,male sex,body mass index>23 kg/m2,presence of metabolic syndrome,current smoking,and alcohol consumption were associated with an increased risk of GERD.Seropositivity for H.pylori immunoglobulin G antibodies was associated with a decreased risk of GERD.There was an inverse correlation between the extent of EAG and occurrence of GERD:Odds ratio(OR),1.01[95%confidence interval(CI):0.90-1.14]in C1,0.87(0.78-0.97)in C2,0.71(0.62-0.80)in C3,0.52(0.44-0.61)in O1,0.37(0.29-0.48)in O2,and 0.28(0.18-0.43)in O3.Additionally,the extent of EAG showed an inverse correlation with the severity of GERD.The presence of SAG was correlated with a reduced risk of GERD(OR=0.49,95%CI:0.28-0.87,P=0.014).CONCLUSION The extent of EAG and SAG exhibited strong inverse relationships with the occurrence and severity of GERD.AG followed by H.pylori infection may be independently protect against GERD.     

Serum gastrin and pepsinogen in shift workers

Summary Gastrointestinal complaints, including peptic ulcer, are believed to be associated and enhanced by shift work (SW). However, there are no clear reports in the literature about this acquired pathology. Serum gastrin (G) and group I pepsinogen (PG1) are thought to play a role in the pathogenesis of peptic ulcer and may be considered a useful test of the gastric function. Five adult male foundry shift workers, without any demonstrated gastrointestinal pathology, were studied over a month's span during the following weekly rotating shift schedule: 07.45–16.45, 06.00–14.00, 14.00–22.00, 22.00–06.00. Six adult, day-working males acted as controls. Blood samples drawn at the beginning and at the end of each weekly shift were assayed for G and PG1 utilizing RIA kits. Our data showed that SW causes a prominent change in the gastrin/acidopepsin secretion system.     

Immunohistochemical localization of pepsinogen A and C containing cells in Barrett's oesophagus

Summary No data are available on the localization of Pepsinogen A (PGA=PG I) and Pepsinogen C (PGC=PG II) positive cells in Barrett's epithelium. Endoscopic biopsy specimens were taken from the columnar epithelium from 23 patients (n=93), and in addition from the cardia from eight healthy control subjects (n=38). The tissue was stained by the immunoperoxidase technique with specific anti-pepsinogen antisera, and double immunostained for PGA and PGC. In the Barrett's epithelium PGA was found in 28 out of 93 biopsy specimens (30.1%) and PGC in 55 out of 93 (59.1%). Chief cells always stained both for PGA and PGC, while clear mucous cells were often PGA– and PGC+. PGA+ and PGC+ cells were found each in 100% of the biopsy specimens with fundic type epithelium, in 21.7% and 70.7% of biopsy specimens with junctional type, in 0% and 26.1% of biopsy specimens with specialized epithelium and in 12.5% and 43.5% of biopsy specimens with mixed junctional/specialized features respectively. Dysplastic epithelium stained always negatively with both anti-pepsinogen antisera. In most control cardia biopsy specimens PGA as well as PGC were demonstrable; occasionally clear mucous glands were PGA– and PGC+.It is concluded that pepsinogen-containing cells can be accurately identified in the Barrett's epithelium; their presence seems related to the histological cell type. Identification of pepsinogen positive cells may contribute to a more accurate morphological classification of the Barrett's epithelium.Presented in part at the Annual Meeting of the American Gastroenterological Association, San Francisco, May 1986     

Helicobacter pylori clearance and serum gastrin and pepsinogen I concentrations in omeprazole treatment of duodenal ulcer patients

Objective: To determine which demographic factors may influence serum gastrin and pepsinogen I (PGI) levels in duodenal ulcer patients undergoing omeprazole treatment. Methods: We conducted an outpatient-based prospective study in the Veterans General Hospital, Taipei, to investigate the pharmacological effects on patients with duodenal ulcers receiving omeprazole treatment for 4 weeks. Sixty-eight patients (61 males/7 females, aged 25–73 years) with endoscopically confirmed duodenal ulcer were included. Gastrin and pepsinogen I levels were measured before and after treatment. Demographic factors including age, sex, smoking, ulcer healing and antral Helicobacter pylori colonization/clearance were analyzed, in order to measure their probable influences on serum gastrin and pepsinogen I levels. Results: Ulcer healing was seen in 92.6% of patients while 48 (70.6%) antral clearances were seen in 66 H. pylori colonized patients at the end of trial. Omeprazole monotherapy led to a marked elevation of serum gastrin (85.8 pg · ml⁻¹, SD 32.0 pg · ml⁻¹ vs 133.9 pg · ml⁻¹, SD 71.6 pg · ml⁻¹, P < 0.01), and pepsinogen I (111.0 ng · ml⁻¹, SD 36.7 ng · ml⁻¹ vs 253.6 ng · ml⁻¹, SD 64.8 ng · ml⁻¹, P < 0.01) levels when measured on day 29. Only patients showing antral H. pylori clearance exhibited an influence on the magnitude of pepsinogen I elevation following omeprazole monotherapy (143.9%, SD 67.3% vs 78.6%, SD 51.2%, P < 0.01). Moreover, the sensitivity and specificity of serum pepsinogen I variations were plotted on a receiving operating characteristic (ROC) curve. The 140% increased pepsinogen I level yielded a maximum accuracy of 80% specificity or 50% sensitivity to predict antral H. pylori clearance. Conclusion: Antral H. pylori clearance is at least partially responsible for the omeprzaole-induced hyperpepsinogenemia I. The magnitude of hyperpepsinogenemia I probably provides a non-invasive alternative for predicting H. pylori clearance. Received: 22 August 1996 / Accepted in revised form: 1 October 1998     

胃蛋白酶原及胃泌素17对胃癌及癌前病变的诊断价值

目的探讨外周血胃蛋白酶原(PG)Ⅰ、PGⅡ及胃泌素17(G-17)对胃癌及癌前病变的诊断价值。方法采用回顾性研究方法,收集南通大学附属南京江北医院2019年1月1日至12月31日的268例住院的胃癌(胃癌组19例)、癌前病变(癌前病变组126例)及非萎缩性胃炎(非萎缩性胃炎组123例)患者,癌前病变组又分为萎缩性胃炎组(34例)、萎缩性胃炎伴肠化组(86例)、萎缩性胃炎伴异型增生组(6例)三个亚组,采取荧光免疫层析法检测各组外周血G-17水平,酶联免疫法检测各组外周血PGⅠ、PGⅡ,比较其差异,并评估PGⅠ、PGⅡ和两者比值(PGR)及G-17与胃癌及癌前病变风险的相关性。结果三组中的PGⅠ、PGR、G-17水平差异有统计学意义(P<0.01),其中,胃癌组的PGⅠ、PGR水平较非萎缩性胃炎组、癌前病变组减低,G-17值较非萎缩性胃炎组、癌前病变组增高,差异均有统计学意义(P<0.05);仅PGⅡ水平在癌前病变组三个亚组间差异有统计学意义(P<0.05)。ROC曲线分析示,PGⅠ筛选胃癌的最佳截断值为59.06 ng/ml,其特异度及灵敏度分别为57.9%、86.0%;PGR筛选胃癌的最佳临界值为7.61,其特异度及灵敏度分别为78.9%、69.6%。PGⅠ和G-17联合筛查胃癌的灵敏度及特异度为88.0%、68.4%;PGⅡ联合G-17筛查胃癌灵敏度和特异度分别为83.9%、63.2%;PGR联合G-17筛查胃癌的灵敏度及特异度为62.7%和89.5%。结论PGⅠ、PGR可作为胃癌及癌前病变的筛查指标,PGⅠ、PGⅡ、PGR分别与G-17联合检测,可提高预测价值,但在与萎缩性胃炎是否伴有肠化及异型增生之间无明显相关性。     

养胃颗粒联合四联疗法治疗Hp阳性慢性胃炎的疗效

目的探讨养胃颗粒联合四联抗菌法治疗Hp阳性慢性胃炎的疗效及其安全性。方法选取2018年12月至2019年12月Hp相关性慢性胃炎患者120例,按照随机数字法分为对照组和观察组,各60例。对照组给予四联疗法,观察组给予养胃颗粒联合四联疗法,比较两组患者治疗有效率、Hp根除率、血液指标变化及不良反应情况。结果观察组临床治疗总有效率、Hp根除率、血清GAS水平、血清PGⅠ水平和PGⅠ/PGⅡ比值均高于对照组,差异有统计学意义(P<0.05)。结论养胃颗粒联合四联抗菌法治疗Hp阳性慢性胃炎的临床效果更优越,能显著提高Hp根除率,并可以减少消化道不良反应和肝损病例。     

胃蛋白酶原，胃泌素测定在胃癌诊断中的应用研究

[目的]探讨胃蛋白酶原Ⅰ（PGⅠ）、胃蛋白酶原Ⅱ（PGⅡ）、胃泌素（GS）水平变化对胃癌的诊断价值。[方法]应用免疫放射分析法测定了100例正常人，66例胃癌、107例胃溃疡，101例慢性胃炎患者血清PGⅠ、PGⅡ、GS含量及PGⅠ／PGⅡ比值的变化。[结果]胃癌组血清PGⅠ、PGI／PGⅡ水平较对照组显著降低（〈0．001），PGⅡ水平较对照组无显著变化（P〉0．05），GS水平较对照、慢性胃炎组和溃疡病组组明显增高（P〈0．001）。[结论]血清PGⅠ和PGⅠ／PGⅡ比值下降，GS增高是与胃癌发生密切相关的高危因素，可作为诊断胃癌的一项血清学指标，对胃癌的诊断有一定的临床意义。     

胃蛋白酶原对儿童幽门螺杆菌相关胃炎诊断价值的研究

目的探讨胃蛋白酶原(PG)与幽门螺杆菌(HP)相关胃炎的关系及其诊断价值。方法对82例以上消化道症状就诊儿童进行PG检测,与胃镜结果对比,通过受试者工作特征曲线对PG诊断价值进行评价。结果 HP阳性组PGⅠ、PGⅡ水平明显升高,PGⅠ/PGⅡ降低。PGⅡ≥9.01μg/L的检出灵敏度和特异度分别为96.7%和75%。结论 PG水平与胃炎患儿HP感染状态密切相关。PGⅡ≥9.01μg/L可以作为辅助诊断儿童幽门螺杆菌相关胃炎的非侵入性指标。     

Differences in the Levels of Gastric Cancer Risk Factors Between Nanjing and Minqing Counties,China

Objectives:

In Fujian Province, China, gastric cancer is one of the leading causes of mortality among all malignant tumors. Nanjing county and Minqing county are located in inland Fujian and have similar general demographics. However, the adjusted mortality rate of gastric cancer in Minqing was found to be much higher than that in Nanjing. We sought to explore factors associated with this increased risk of gastric cancer between the two counties.

Methods:

We recruited 231 and 224 residents from Nanjing and Minqing, respectively, and analyzed differences between their dietary habits, Helicobacter pylori infection rates, and concentrations of serum pepsinogen I, pepsinogen II, gastrin-17, and ratio of pepsinogen I:II.

Results:

Subjects in Minqing had more first-degree relatives who had been diagnosed with upper gastrointestinal tumor, more unhealthy dietary habits, a higher Helicobacter pylori positive rate, and greater proportion of abnormal serum gastrin-17 than those in Nanjing did.

Conclusions:

The factors that differed between these two counties might indicate that residents in Minqing have a higher risk for developing gastric cancer than those in Nanjing do.     

Presence of Gastric Autoantibodies Impairs Gastric Secretory Function in Patients with Helicobacter pylori-positive Duodenal Ulcer

Background: Although the association between Helicobacter pylori infection and gastric autoimmunity is now well established, to date little is known about the significance of anticanalicular autoantibodies in patients with duodenal ulcer (DU). We therefore investigated the prevalence of serum antiparietal cell autoreactivity in DU patients as well as the relationship between these autoantibodies, gastric histopathology and gastric secretory function in this setting. Methods: Forty-one consecutive patients with H. pylori-positive DU were initially recruited. In all patients, basal (BAO) and pentagastrin stimulated acid output (PAO), fasting and meal-induced serum gastrin levels, as well as serum pepsinogen I concentrations, were measured. Antral and body gastritis was evaluated according to the Sydney system. Serum anticanalicular autoreactivity was determined by the indirect immunoperoxidase technique. Results: Serum anticanalicular autoantibodies were found in 7 out of 34 patients (20%). The presence of these antibodies was associated with a significantly higher grade of body gastritis (activity: 1.9 versus 0.9) as well as with significantly higher fasting and meal stimulated gastrin levels (mean fasting gastrin, 76.4 (15.2) pg/ml versus 59.3 (20.5) pg/ml). In addition, PAO values were significantly lower in patients with gastric autoantibodies than in those without this autoreactivity (mean 0.35 (0.16) mmol kg^-1 h^-1 versus 0.49 (0.16) mmol kg^-1 h^-1). In contrast, no significant differences were found between patients with and without anticanalicular autoantibodies as regards fasting serum pepsinogen I concentrations. Conclusions: Serum anticanalicular autoantibodies can be detected in 20% of patients with DU and are associated with a more severe pattern of body gastritis, higher gastrin levels and decreased peak acid secretion values. Their presence could account for the normal or reduced acid output which can be seen in a subset of DU patients.